Following on from the previous two chapters presents an obituary for Ward Edwards. Ward's 1954 paper in the Psychological Bulletin introduced decision making as a research topic for psychologists. He ...
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Following on from the previous two chapters presents an obituary for Ward Edwards. Ward's 1954 paper in the Psychological Bulletin introduced decision making as a research topic for psychologists. He continued to make significant contributions to the field for more than fifty years, contributing some 200 publications to the literature. He died from Parkinson's Disease on February 1, 2005.Less

Obituary

David J WeissJames Shanteau

Published in print: 2008-10-10

Following on from the previous two chapters presents an obituary for Ward Edwards. Ward's 1954 paper in the Psychological Bulletin introduced decision making as a research topic for psychologists. He continued to make significant contributions to the field for more than fifty years, contributing some 200 publications to the literature. He died from Parkinson's Disease on February 1, 2005.

Our ability to map and intervene in the structure of the human brain is proceeding at a very quick rate. Advances in psychiatry, neurology, and neurosurgery have given us fresh insights into the ...
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Our ability to map and intervene in the structure of the human brain is proceeding at a very quick rate. Advances in psychiatry, neurology, and neurosurgery have given us fresh insights into the neurobiological basis of human thought and behavior. Technologies like MRI and PET scans can detect early signs of psychiatric disorders before they manifest symptoms. Electrical and magnetic stimulation of the brain can non-invasively relieve symptoms of obsessive-compulsive disorder, depression, and other conditions resistant to treatment, while implanting neuro-electrodes can help patients with Parkinson's and other motor control-related diseases. New drugs can help regenerate neuronal connections otherwise disrupted by schizophrenia and similar diseases. All these procedures and drugs alter the neural correlates of our mind, and raise fascinating and important ethical questions about their benefits and harms. They are, in a sense, among the most profound bioethical questions we face, since these techniques can touch on the deepest aspects of the human mind: free will, personal identity, the self, and the soul. This book starts by describing the state of the art in neuroscientific research and treatment, and gives an up-to-date picture of the brain. It then looks at the ethical implications of various kinds of treatments, such as whether or not brain imaging will end up changing our views on free will and moral responsibility; whether patients should always be told that they are at future risk for neurological diseases; if erasing unconscious emotional memories implicated in depression can go too far; if forcing behavior-modifying drugs or surgery on violent offenders can ever be justified; the implications of drugs that enhance cognitive abilities; and how to define brain death and the criteria for the withdrawal of life–support.Less

Bioethics and the Brain

Walter Glannon

Published in print: 2006-12-07

Our ability to map and intervene in the structure of the human brain is proceeding at a very quick rate. Advances in psychiatry, neurology, and neurosurgery have given us fresh insights into the neurobiological basis of human thought and behavior. Technologies like MRI and PET scans can detect early signs of psychiatric disorders before they manifest symptoms. Electrical and magnetic stimulation of the brain can non-invasively relieve symptoms of obsessive-compulsive disorder, depression, and other conditions resistant to treatment, while implanting neuro-electrodes can help patients with Parkinson's and other motor control-related diseases. New drugs can help regenerate neuronal connections otherwise disrupted by schizophrenia and similar diseases. All these procedures and drugs alter the neural correlates of our mind, and raise fascinating and important ethical questions about their benefits and harms. They are, in a sense, among the most profound bioethical questions we face, since these techniques can touch on the deepest aspects of the human mind: free will, personal identity, the self, and the soul. This book starts by describing the state of the art in neuroscientific research and treatment, and gives an up-to-date picture of the brain. It then looks at the ethical implications of various kinds of treatments, such as whether or not brain imaging will end up changing our views on free will and moral responsibility; whether patients should always be told that they are at future risk for neurological diseases; if erasing unconscious emotional memories implicated in depression can go too far; if forcing behavior-modifying drugs or surgery on violent offenders can ever be justified; the implications of drugs that enhance cognitive abilities; and how to define brain death and the criteria for the withdrawal of life–support.

This book reviews a number of clinical neuropsychiatric conditions in which brain oscillations play an essential role. It discusses how the intrinsic properties of neurons, and the interactions ...
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This book reviews a number of clinical neuropsychiatric conditions in which brain oscillations play an essential role. It discusses how the intrinsic properties of neurons, and the interactions between neurons – mediated by both chemical synapses and by gap junctions – can lead to oscillations in populations of cells. The discussion is based largely on data derived from in vitro systems (hippocampus, cerebral and cerebellar cortex) and from network modeling. Finally, the book considers how brain oscillations can provide insight into normal brain function as well as pathophysiology.Less

Cortical Oscillations in Health and Disease

Roger Traub, MDMiles Whittington, PhD

Published in print: 2010-04-14

This book reviews a number of clinical neuropsychiatric conditions in which brain oscillations play an essential role. It discusses how the intrinsic properties of neurons, and the interactions between neurons – mediated by both chemical synapses and by gap junctions – can lead to oscillations in populations of cells. The discussion is based largely on data derived from in vitro systems (hippocampus, cerebral and cerebellar cortex) and from network modeling. Finally, the book considers how brain oscillations can provide insight into normal brain function as well as pathophysiology.

For modern scientists, history often starts with last week's journals and is regarded as largely a quaint interest compared with the advances of today. However, this book makes the case that, ...
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For modern scientists, history often starts with last week's journals and is regarded as largely a quaint interest compared with the advances of today. However, this book makes the case that, measured by major advances, the greatest decade in the history of brain studies was mid-twentieth century, especially the 1950s. The first to focus on worldwide contributions in this period, this book ranges through dozens of astonishing discoveries at all levels of the brain, from DNA (Watson and Crick), through growth factors (Hamburger and Levi-Montalcini), excitability (Hodgkin and Huxley), synapses (Katz and Eccles), dopamine and Parkinson's (Carlsson), visual processing (Hartline and Kuffler), the cortical column (Mountcastle), reticular activating system (Morruzzi and Magoun) and REM sleep (Aserinsky), to stress (Selye), learning (Hebb) and memory (HM and Milner). The clinical fields are also covered — from Cushing and Penfield, psychosurgery, and brain energy metabolism (Kety), to most of the major psychoactive drugs in use today (beginning with Delay and Deniker) — and much more. There is a focus on the creative process itself; on understanding how the combination of unique personalities, innovative hypotheses, and new methods led to the advances. Insight is given into this process through describing the struggles between male and female, student and mentor, academic and private sector, and the roles of chance and persistence. The book thus provides a multidisciplinary understanding of the revolution that created the modern field of neuroscience, and which set the bar for judging current and future advances.Less

Creating Modern Neuroscience: The Revolutionary 1950s

Gordon M. Shepherd MD, DPhil

Published in print: 2009-09-30

For modern scientists, history often starts with last week's journals and is regarded as largely a quaint interest compared with the advances of today. However, this book makes the case that, measured by major advances, the greatest decade in the history of brain studies was mid-twentieth century, especially the 1950s. The first to focus on worldwide contributions in this period, this book ranges through dozens of astonishing discoveries at all levels of the brain, from DNA (Watson and Crick), through growth factors (Hamburger and Levi-Montalcini), excitability (Hodgkin and Huxley), synapses (Katz and Eccles), dopamine and Parkinson's (Carlsson), visual processing (Hartline and Kuffler), the cortical column (Mountcastle), reticular activating system (Morruzzi and Magoun) and REM sleep (Aserinsky), to stress (Selye), learning (Hebb) and memory (HM and Milner). The clinical fields are also covered — from Cushing and Penfield, psychosurgery, and brain energy metabolism (Kety), to most of the major psychoactive drugs in use today (beginning with Delay and Deniker) — and much more. There is a focus on the creative process itself; on understanding how the combination of unique personalities, innovative hypotheses, and new methods led to the advances. Insight is given into this process through describing the struggles between male and female, student and mentor, academic and private sector, and the roles of chance and persistence. The book thus provides a multidisciplinary understanding of the revolution that created the modern field of neuroscience, and which set the bar for judging current and future advances.

In Parkinson's disease (PD), dopamine (DA) neurons in the substantia nigra pars compacta (SNc) progressively degenerate. This disruption in nigrostriatal DA transmission results in many motor abnormalities. A number of neurotoxins have been used to induce DA cell loss to model PD, with the most extensively studied models being 6-hydroxydopamine (6-OHDA) in the rat and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the mouse. More recently, the discovery of genetic forms of PD has led to the development of genetic mouse models of parkinsonism. In all models, sensorimotor tests that are sensitive to dysfunction and loss of nigrostriatal DA neurons have been developed to provide important endpoint measures for preclinical testing of potential therapeutic treatments for PD. This chapter reviews many of the tests used in the unilateral 6-OHDA rat and in mice with mutations associated with PD and/or the development of DA neurons.Less

Dopamine and Motor Function in Rat and Mouse Models of Parkinson’s Disease

Timothy SchallertSheila M. Fleming

Published in print: 2009-10-16

In Parkinson's disease (PD), dopamine (DA) neurons in the substantia nigra pars compacta (SNc) progressively degenerate. This disruption in nigrostriatal DA transmission results in many motor abnormalities. A number of neurotoxins have been used to induce DA cell loss to model PD, with the most extensively studied models being 6-hydroxydopamine (6-OHDA) in the rat and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the mouse. More recently, the discovery of genetic forms of PD has led to the development of genetic mouse models of parkinsonism. In all models, sensorimotor tests that are sensitive to dysfunction and loss of nigrostriatal DA neurons have been developed to provide important endpoint measures for preclinical testing of potential therapeutic treatments for PD. This chapter reviews many of the tests used in the unilateral 6-OHDA rat and in mice with mutations associated with PD and/or the development of DA neurons.

Dopamine (DA) has long been known to be a critical modulator of striatal processing of cortical and thalamic signals carried by glutamatergic synapses on the principal neurons of the striatum—medium ...
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Dopamine (DA) has long been known to be a critical modulator of striatal processing of cortical and thalamic signals carried by glutamatergic synapses on the principal neurons of the striatum—medium spiny neurons (MSNs). Dopamine regulation of these neurons is important for an array of psychomotor functions ascribed to the basal ganglia, including associative learning and action selection. This chapter focuses on four topics: (1) the intrinsic differences between MSNs expressing D1 and D2 dopamine receptors; (2) how DA modulates postsynaptic properties that influence glutamatergic synaptic events and their integration by MSNs in the dorsal striatum; (3) how DA influences the induction of long-term synaptic plasticity; and (4) how DA depletion in Parkinson's disease (PD) models remodels glutamatergic signaling.Less

Published in print: 2009-10-16

Dopamine (DA) has long been known to be a critical modulator of striatal processing of cortical and thalamic signals carried by glutamatergic synapses on the principal neurons of the striatum—medium spiny neurons (MSNs). Dopamine regulation of these neurons is important for an array of psychomotor functions ascribed to the basal ganglia, including associative learning and action selection. This chapter focuses on four topics: (1) the intrinsic differences between MSNs expressing D1 and D2 dopamine receptors; (2) how DA modulates postsynaptic properties that influence glutamatergic synaptic events and their integration by MSNs in the dorsal striatum; (3) how DA influences the induction of long-term synaptic plasticity; and (4) how DA depletion in Parkinson's disease (PD) models remodels glutamatergic signaling.

This chapter addresses nine myths about Parkinson's disease (PD). Among these are the myths that PD is a movement disorder characterized by the classic triad of akinesia, rigidity, and tremor; that ...
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This chapter addresses nine myths about Parkinson's disease (PD). Among these are the myths that PD is a movement disorder characterized by the classic triad of akinesia, rigidity, and tremor; that first symptoms appear in the patient's 60s; and that clinical diagnosis is simple. It argues that the symptoms of PD are often hidden in plain sight because we have become accustomed to think of this disease in certain slightly calcified ways. However, pathophysiological and therapeutic progress constantly challenges our understanding of PD and, ultimately, the approach to patient diagnosis and care. Although PD remains the paradigmatic dopaminergic disease, we now appreciate that it is a multisystem brain disorder. More importantly, understanding PD—and other chronic neurodegenerative disorders—depends heavily on a precise semiologic analysis of each individual patient. Semiology, then, is the key to understanding brain function and dysfunction.Less

Exploring the Myths about Parkinson’s Disease

Yves AgidAndreas Hartmann

Published in print: 2009-10-16

This chapter addresses nine myths about Parkinson's disease (PD). Among these are the myths that PD is a movement disorder characterized by the classic triad of akinesia, rigidity, and tremor; that first symptoms appear in the patient's 60s; and that clinical diagnosis is simple. It argues that the symptoms of PD are often hidden in plain sight because we have become accustomed to think of this disease in certain slightly calcified ways. However, pathophysiological and therapeutic progress constantly challenges our understanding of PD and, ultimately, the approach to patient diagnosis and care. Although PD remains the paradigmatic dopaminergic disease, we now appreciate that it is a multisystem brain disorder. More importantly, understanding PD—and other chronic neurodegenerative disorders—depends heavily on a precise semiologic analysis of each individual patient. Semiology, then, is the key to understanding brain function and dysfunction.

This chapter begins with a discussion of motor complications of L-DOPA pharmacotherapy. It then discusses animal models of treatment-induced motor complications and the multilayered pathophysiology ...
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This chapter begins with a discussion of motor complications of L-DOPA pharmacotherapy. It then discusses animal models of treatment-induced motor complications and the multilayered pathophysiology of L-DOPA-induced dyskinesia, presynaptic changes in DA release and clearance, imbalance in the activity of striatal efferent pathways, altered plasticity of corticostriatal synapses, altered activity in peptidergic and GABAergic pathways to the basal ganglia output nuclei, and system-level changes in cortico-basal ganglionic circuits.Less

Pathophysiology of L-DOPA-Induced Dyskinesia in Parkinson's Disease

M. Angela Cenci

Published in print: 2009-10-16

This chapter begins with a discussion of motor complications of L-DOPA pharmacotherapy. It then discusses animal models of treatment-induced motor complications and the multilayered pathophysiology of L-DOPA-induced dyskinesia, presynaptic changes in DA release and clearance, imbalance in the activity of striatal efferent pathways, altered plasticity of corticostriatal synapses, altered activity in peptidergic and GABAergic pathways to the basal ganglia output nuclei, and system-level changes in cortico-basal ganglionic circuits.

This chapter discusses imaging studies of Parkinson's disease (PD). Imaging dopaminergic function with positron emission tomography (PET) and single photon computed emission tomography (SPECT) or changes in the expression of a PD-related profile (PDRP) with 18F-fluorodeoxyglucose (FDG) PET currently remain the best biomarkers for monitoring disease progression. These measurements correlate significantly with clinical disability in PD and are able to detect preclinical dysfunction. However, the modalities cannot be regarded as surrogate markers as they do not correlate well with clinical outcome in practice, and may well be directly influenced by medication changes. While structural changes in PD substantia nigra can be detected with transcranial sonograpy (TCS), the associated hyperechogenicity does not appear to alter as patients clinically deteriorate. Volumetric magnetic resonance imaging (MRI) is valuable for detecting progressive brain atrophy in PD patients who developed later dementia, but currently is unable to detect nigral volume changes.Less

Progression of Parkinson’s Disease Revealed by Imaging Studies

David J. Brooks

Published in print: 2009-10-16

This chapter discusses imaging studies of Parkinson's disease (PD). Imaging dopaminergic function with positron emission tomography (PET) and single photon computed emission tomography (SPECT) or changes in the expression of a PD-related profile (PDRP) with 18F-fluorodeoxyglucose (FDG) PET currently remain the best biomarkers for monitoring disease progression. These measurements correlate significantly with clinical disability in PD and are able to detect preclinical dysfunction. However, the modalities cannot be regarded as surrogate markers as they do not correlate well with clinical outcome in practice, and may well be directly influenced by medication changes. While structural changes in PD substantia nigra can be detected with transcranial sonograpy (TCS), the associated hyperechogenicity does not appear to alter as patients clinically deteriorate. Volumetric magnetic resonance imaging (MRI) is valuable for detecting progressive brain atrophy in PD patients who developed later dementia, but currently is unable to detect nigral volume changes.

This chapter reviews the transplantation of dopamine (DA) neurons as a powerful model for understanding the basic neurobiology and methods for achieving viable cell transplantation in the brain. ...
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This chapter reviews the transplantation of dopamine (DA) neurons as a powerful model for understanding the basic neurobiology and methods for achieving viable cell transplantation in the brain. Analysis of the mechanisms involved in structural repair and functional recovery indicates that there are particular requirements for the implanted cells to differentiate into specific brainstem phenotypes for effective integration into the host brain and broad functionally efficacy. Cell implantation into DA-denervated rats and mice has provided effective animal models for the preclinical analyses required for translating novel cell therapies into applications in human neurodegenerative disease and for resolving specific issues, such as potential dyskinetic side effects, that have been raised in the course of the pilot clinical trials.Less

Transplantation of Dopamine Neurons: Extent and Mechanisms of Functional Recovery in Rodent Models of Parkinson's Disease

Stephen B. DunnettAnders Björklund

Published in print: 2009-10-16

This chapter reviews the transplantation of dopamine (DA) neurons as a powerful model for understanding the basic neurobiology and methods for achieving viable cell transplantation in the brain. Analysis of the mechanisms involved in structural repair and functional recovery indicates that there are particular requirements for the implanted cells to differentiate into specific brainstem phenotypes for effective integration into the host brain and broad functionally efficacy. Cell implantation into DA-denervated rats and mice has provided effective animal models for the preclinical analyses required for translating novel cell therapies into applications in human neurodegenerative disease and for resolving specific issues, such as potential dyskinetic side effects, that have been raised in the course of the pilot clinical trials.